Effects of colchicine on amoeboid microglial cells in the postnatal rat brain.

The present study was conducted to examine the response of amoeboid microglial cells in the postnatal rat brain to colchicine administration. One-day-old postnatal rats were given intraperitoneal injections of colchicine and sacrificed at 7, 14 and 21 days of age. In rats killed at 7 days age, the number of OX-42, OX-18 and ED1 positive amoeboid microglial cells was considerably reduced when compared with the control rats. At 14 and 21 days, the number of cells immunoreactive with the above antibodies was comparable to that of the control rats. The intensity of the immunoreaction with the various antibodies was also comparable in colchicine injected and control rats. When rhodamine isothiocyanate (RhIC) was administered, amoeboid microglial cells emitted a bright fluorescence in control rats as well as in colchicine-injected rats, although in the latter, the number of RhIC labelled cells was considerably reduced. With the antibody bromodeoxyuridine a large number of stained cells were observed in the control rats. On the other hand, occasional labelled cells were recognized in colchicine-injected rats. Apoptotic amoeboid microglial cells were observed in 4-day-old colchicine-injected rats. At the electron microscopic level, amoeboid microglial cells in colchicine-injected rats killed at 7 days of age showed a large number of phagosomes in their cytoplasm compared with the corresponding control rats. At 14 and 21 days, in colchicine-injected and control rats, amoeboid microglial cells did not display any noticeable differences. It is concluded from the present study that colchicine suppresses the number of amoeboid microglial cells, and that this may be attributed to the antimitotic effect of the drug as well as apoptosis induced by it; the phagocytic activity, however, was not affected. The cells returned to their normal population and morphological features once the drug was discontinued, indicating the reversible nature of the drug effect.